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Y T Kim

Publications and source records attributed to Y T Kim.

At least 163 records · Page 9Linked to original sources
PubMed1985

An immunochemical study of the pyruvate dehydrogenase deficit in Alzheimer's disease brain.

The activity of the pyruvate dehydrogenase complex (PDHC; EC 1.2.4.1, EC 2.3.1.12, and EC 1.6.4.3) was reduced to about 30% of control values in histologically unaffected occipital cortex of the brains of patients with Alzheimer's disease, as well as in histologically affected frontal cortex. In contrast, activity of another mitochondrial enzyme, glutamate dehydrogenase, was normal. Neither age nor time until postmortem study correlated significantly with PDHC activity in either Alzheimer or control samples, and PDHC was not inactivated significantly on incubation with homogenates of either Alzheimer or control brain. Antibodies against the highly purified bovine PDHC inhibited Alzheimer and control PDHC equally per unit of enzyme activity. Immunoblots also indicated that the PDHC antigens were not different in normal and Alzheimer brains. This antibody, however, inhibited Alzheimer PDHC more effectively than it did control PDHC, based on milligrams of protein, suggesting a reduced amount of normal PDHC protein. Other data suggest that the PDHC deficiency is related to mitochondrial damage and to impaired calcium homeostasis in Alzheimer nerve cells, which may then mediate a variety of other cellular impairments.

Aged↗
PubMed1985

Immunochemical characterization of pyruvate dehydrogenase complex in rat brain.

Pyruvate dehydrogenase complex (PDHC) in rat brain was studied immunochemically, using antibodies against the bovine kidney PDHC, by immunoblotting, immunoprecipitation, inhibition of enzyme activity, and enzyme-linked immunoabsorbent assay (ELISA). The immunoblots showed that the antibodies bound strongly to the alpha peptide of the pyruvate dehydrogenase (E1) component, and to the dihydrolipoyl transacetylase (E2) and the dihydrolipoyl dehydrogenase (E3) components of PDHC. A similar immunoblotting pattern was observed in all eight brain regions examined. On immunoblotting of the subcellular fractions, these PDHC peptides were observed in mitochondria and synaptosomes but not in the postmitochondrial supernatants. This agrees with other evidence that brain PDHC is localized in the mitochondria. These results, together with those from sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the immunoprecipitin, also showed that the alpha E1, beta E1, and E3 peptides of rat brain PDHC are very similar in sizes to those of the bovine kidney PDHC, being 42, 36, and 58 kD, respectively. The size of the E2 peptide, 66 kD, is different from that of bovine kidney E2, 73 kD. The relative abundance of PDHC protein in nonsynaptic mitochondria was compared by enzyme activity titration and ELISA. Both methods demonstrated that the amount of PDHC antigen in the mitochondria from cerebral cortex is greater than that in the olfactory bulb mitochondria. This is consistent with the results of the activity measurement. The ELISA also showed that the PDHCs in both mitochondrial populations are antigenically similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Plaque-forming cell response of human blood lymphocytes. III. Cellular basis of the reduced immune response in the elderly.

The cellular basis for the reduced immune response of the elderly was studied in vitro. It was found that, with respect to the capacity to respond to relatively T-independent B cell activators by proliferation and generation of plaque-forming cells (PFC), the purified B cell population of aged subjects is relatively intact. Furthermore, macrophages from old and young subjects produce T cell-replacing factors in equivalent amounts. The depressed proliferation and PFC responses to B cell activators in unfractionated lymphocytes from the elderly thus appear to be due to suppressor activity present in a surface Ig-negative cell population, suggesting that alterations in the regulatory (helper and suppressor) functions of T cell populations are the major cause of the reduced humoral immune response associated with aging.

Adult↗
PubMed1984

Studies on the bovine brain pyruvate dehydrogenase complex using the antibodies against kidney enzyme complex.

Pyruvate dehydrogenase complex (PDHC) was purified from bovine kidney with a specific activity of 12-16 mumol of NADH or acetyl-CoA formed/min/mg protein. The four peptides comprising its three catalytic components were separated by sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Rabbit antibodies against this highly purified PDHC (anti-PDHC) exhibited similar binding affinity to the phospho-PDHC as it did to the PDHC antigen. To test whether there exist brain isozymes of PDHC differing from kidney enzyme, which has been extensively characterized, the PDHCs in bovine brain and kidney were compared using this anti-PDHC. The PDHC activities in the brain and kidney mitochondrial extracts were inhibited to the same degree by varying amounts of anti-PDHC. Brain PDHC was precipitated with the anti-PDHC and resolved by SDS-PAGE. The four brain PDHC peptides isolated immunochemically with anti-PDHC had the same sizes as the kidney PDHC peptides. These PDHC peptides from kidney and brain were further compared by their peptide fragment patterns, which were generated by partial proteolysis with Staphylococcus aureus V8 protease or by CNBr and resolved by SDS-PAGE. The peptide patterns generated with the former method indicated that the alpha and beta peptides of the pyruvate dehydrogenase (E1) component and the peptide of dihydrolipoyl transacetylase (E2) component of kidney PDHC were very similar to the corresponding peptides immunologically isolated from brain. The peptide patterns generated with CNBr further confirmed that the beta E1 and E2 peptides of kidney PDHC were similar to the corresponding peptides from brain.

Animals↗
PubMed1984

Cefoperazone (Cefobid) for treating men with gonorrhoea caused by penicillinase producing Neisseria gonorrhoeae.

The recent emergence of spectinomycin resistant penicillinase producing Neisseria gonorrhoeae (PPNG) and the high prevalence of PPNG strains among the gonococcal isolates in Seoul represent a grave challenge to the programme for controlling sexually transmitted disease (STD). Fifty men with uncomplicated gonococcal urethritis caused by PPNG strains were treated with a single intramuscular injection of 1 g cefoperazone. Forty two patients were followed up. All patients recovered including three who became reinfected and required further treatment. Two patients (4.8%) developed postgonococcal urethritis (PGU). The MIC90 of cefoperazone measured by an agar dilution susceptibility test was 0.12 mg/l.

Adult↗
PubMed1984

Immunologic studies on the induction of diabetes in experimental animals. Cellular basis for the induction of diabetes by streptozotocin.

Repeated low doses of streptozotocin (STZ, 40 mg/kg body wt) gradually induce hyperglycemia in mice after a latent period of 5-7 days. The ability of STZ to induce hyperglycemia varies in different mouse strains. Repeated low doses of STZ fail to induce diabetes in T-cell-deficient mice, suggesting a crucial role of T-cells in the induction of diabetes by this procedure. Transfer of spleen cells from mice rendered diabetic by repeated low doses of STZ failed to induce hyperglycemia in the recipients. However, pretreating the recipients with a single low dose of STZ permitted efficient transfer of the diabetic state, suggesting that the immunologic reaction resulting in diabetes was actually specific for an STZ-modified beta cell.

Animals↗
PubMed1984

Effects of nutrition on disease and life span. I. Immune responses, cardiovascular pathology, and life span in MRL mice.

Mice of the autoimmune, lymphoproliferative strain MRL/lpr and the congenic, nonlymphoproliferative strain MRL/n were fed one of six diets from weaning on-ward. These mice were sacrificed at 3 or 5 months of age. Low fat diets resulted in lower cholesterol and higher triglyceride levels than did cholesterol-containing high-fat diets. Caloric restriction of MRL/lpr mice was associated with an increased plaque-forming cell response to trinitrophenylated polyacrylamide beads, less lymphoproliferation, and less severe glomerulonephritis. Diet did not affect the incidence of autoimmune vasculitis in MRL/lpr mice sacrificed at 5 months. MRL/lpr mice fed a low-fat, calorically restricted diet from 5 months of age to death lived longer than mice which were fed ad libitum a cholesterol-containing, high-fat diet. At death, MRL/lpr mice fed the former diet had the autoimmune vasculitis which had been evident in mice killed at 5 months, whereas mice fed the latter diet, in addition to the vasculitis, had a high incidence of atherosclerotic lesions of intrarenal and aortic branch arteries.

Animal Nutritional Physiological Phenomena↗
PubMed1984

Cefoperazone for urethritis due to penicillinase-producing Neisseria gonorrhoeae.

Thirty-two men infected with penicillinase-producing Neisseria gonorrhoeae were treated with a single intramuscular dose of 0.5 gm of cefoperazone. Of the 29 patients who were followed up, only two (7%) failed to recover; seven patients (26%) had postgonococcal urethritis. The MICs of cefoperazone were 0.03 microgram/ml (three strains), 0.06 microgram/ml (11), 0.12 microgram/ml (nine), 0.25 microgram/ml (one), and 0.5 microgram/ml (one).

Adult↗
PubMed1982

Induction of insulin-dependent diabetes by streptozotocin. Inhibition by estrogens and potentiation by androgens.

Susceptibility of mice to experimental insulin-dependent diabetes as induced by multiple subdiabetogenic doses of streptozotocin has been shown to be strongly gender-dependent, males being much more susceptible than females. We examined this gender difference further in two strains of genetically susceptible mice to determine whether exogenous steroid sex hormones can both suppress the high susceptibility of males and potentiate the low susceptibility of females. Our results show that, in both BALB/cBOM and C57BL/6 mice, exogenous estrogens can suppress the high susceptibility of males. Conversely, the normally streptozotocin-resistant females become as highly susceptible as males after the administration of androgens. The inhibitory effect of estrogens and the potentiating effect of androgens can be demonstrated after the hormones are given to the mice either chronically (in slow-release capsules implanted at a subcutaneous site), or immediately prior to streptozotocin injection. These observations are consistent with the view that the critical factor that determines the susceptibility of mice to the hyperglycemic effects of streptozotocin is not the absolute concentration of androgens per se, but rather the relative overall level of androgens over estrogens in the recipient animal. Several alternative mechanisms for the effect of sex hormones on diabetogenic sensitivity are discussed.

Androgens↗
PubMed1980

Regulation of immune response in allogeneic mixed spleen cell cultures. I. Influence of I-region on the generation of suppressor cells.

The immune responses of allogeneic mixed spleen cell cultures (MLC) to the T-dependent antigen, SRBC, and to the T-independent antigen, DNP-PAA, were investigated. The immune response to DNP-PAA in MLC with certain strain combinations was always suppressed as compared with the expected PFC response calculated from the PFC responses of the individual strains. This suppression was eliminated by treating the spleen cells with RAMB antiserum plus complement before the incubation of the MLC with DNP-PAA. It can be concluded that the suppression in the PFC response to the T-independent antigen DNP-PAA in MLC is due to the generation of suppressor T-cells. The PFC response to the T-dependent antigen, SRBC, in MLC showed either suppression, no change, or rarely augmenation, suggesting that the allogeneic mixed spleen cell cultures can generate both suppressor and helper T cells and that the balance between helper and suppressor activity regulates the PFC response to a T-dependent antigen. Suppressor activity was also generated in a one-way MLC, but the degree of suppression depended upon which of the two strains was responding. Similar amounts of thymidine were incorporated in the one-way MLR irrespective of which strains was responding. Thus, the extent of proliferation in one-way MLR is not related to the degree of suppressor activity generated. The results further indicate that a difference between two strains in the I-C, S, and G regions of the major histocompatibility complex is required to generate suppressor activitiy that can depress the response to a T-independent antigen, MLC between strains differing in K, I-A, I-B, I-J, I-E, and D regions generate little or no suppressor activity in this system.

Acrylamides↗
PubMed1979

Modification of radiation-induced pulmonary fibrosis in rats.

Male rats received 25 Gy (2,500 rad) of gamma rays to the right hemithorax and were killed three or six months later. Microscopic pulmonary abnormalities developed sooner and progressed more rapidly in animals given control feed than in those given the collagen antagonist D-penicillamine (10 mg/day, p.o.). Three and four months after irradiation, hypoperfusion and radiographic hyperlucency of the right lung were observed in both the treated and control animals.

Animals↗
PubMed1979

Induction of suppressor activity in the autologous mixed lymphocyte reaction and in cultures with concanavalin A.

T lymphocytes that are activated in the autologous mixed lymphocyte reaction (MLR) have suppressor activity. Concanavalin A (Con A) augments the suppressor activity generated in cultures containing both T and non-T lymphocytes and can induce suppressor activity in T-lymphocyte preparations that contain too few (10%) non-T cells to generate a significant autologous MLR. However, when such T-lymphocyte preparations are further depleted of adherent cells and contain less than 2% non-T cells, Con A fails to induce suppressor activity. These findings support the concept that an autologous MLR may play an important role in generation of suppressor cells by Con A.

Antibody Formation↗
PubMed1979

Hyperglycemic factor in submandibular glands and its etiological relations to diabetes mellitus in mice.

Bilateral ligation of both the submandibular and parotid ducts of adult normal and mutant hyperinsulinemic diabetic mice resulted in a significant hypoglycemic effect. Therefore, we postulated that duct ligation may result in the removal of hyperglycemic factor (Hoshino et al., 1976) rather than a change in insulin sensitivity. Indeed, no change in specific binding of 125I-insulin was observed in membrane fractions from several tissues obtained from mice of either sex or strains before and after duct ligation. After slices of the submandibular gland were incubated for 4 hr in Eagle's medium, an aliquot of the culture medium was injected i.p. into normal adult mice. A signigicant hyperglycemic effect was observed in 30 min in the injected animals. Eluates obtained by gel filtration of the crude extract of the submandibular gland were injected into normal adult mice, and hyperglycemia ensued. Thus, it is postulated that ligation of salivary ducts results in glandular atrophy and disappearance of the hyperglycemic factor which in turn leads to hypoglycemia and amelioration of diabetes mellitus, particularly of hyperinsulinemic type.

Animals↗